ArticleThe international journal of biochemistry & cell biology2013
p130Cas acts as survival factor during PMA-induced apoptosis in HL-60 promyelocytic leukemia cells.
Article in The international journal of biochemistry & cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- p130Cas Is Correlated with EREG Expression and a Prognostic Factor Depending on Colorectal Cancer Stage and Localization Reducing FOLFIRI Efficacy.International journal of molecular sciences · 2021Article
- Exosomes mediate intercellular transfer of non-autonomous tolerance to proteasome inhibitors in mixed-lineage leukemia.Cancer science · 2020Article
- A truncated phosphorylated p130Cas substrate domain is sufficient to drive breast cancer growth and metastasis formation in vivo.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- The progress of early growth response factor 1 and leukemia.Intractable & rare diseases research · 2016Review
- Positive Feedback Cycle of TNFα Promotes Staphylococcal Enterotoxin B-Induced THP-1 Cell Apoptosis.Frontiers in cellular and infection microbiology · 2016Article
- Identification of Novel Crk-associated Substrate (p130Cas) Variants with Functionally Distinct Focal Adhesion Kinase Binding Activities.The Journal of biological chemistry · 2015Article
- CAS proteins in health and disease: an update.IUBMB life · 2014Review
- Expression of a phosphorylated substrate domain of p130Cas promotes PyMT-induced c-Src-dependent murine breast cancer progression.Carcinogenesis · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Phorbol 12-myristate 13-acetate (PMA) stimulates the differentiation of promyelocytic leukemia HL-60 cells by inducing adhesion followed by cell aggregation and, importantly, apoptosis. p130Cas (Crk-associated substrate) is an adapter molecule that controls cell growth, attachment and apoptotic programs. Notably, elevated p130Cas activity is associated with leukemias and lymphomas. Since p130Cas regulates cell adhesion, we tested the hypothesis that it participates in the differentiation of hematopoietic cells. Here we show that PMA mediates the late induction of p130Cas expression in HL-60 cells, which coincided with cell aggregation and the onset of apoptosis. Ectopic p130Cas expression led to increased cell adhesion and earlier cell aggregation potentially contributing to the observed increased cell viability in these transductants. p130Cas expression concurred with the induction of its own regulator the transcription factor EGR1, its coregulator NAB2, and apoptosis. NF-κB inhibition in PMA-treated HL-60 cells promoted the loss of cell aggregation and cell death. We further showed a reduction of p130Cas, EGR1, and NAB2 levels in response to NF-κB inhibition during PMA treatment. Hence, p130Cas acts as survival factor by limiting PMA-mediated cell cluster disruption and resulting cell death in HL-60 cells.
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